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Effect of anti-PGE antibody on cell-mediated immune response in thermally injured mice
1Department of Surgery, University of Utah Medical Center, Salt Lake City.
Prostaglandin E (PGE) production is elevated in burn-injured individuals and has been implicated as a mechanism in thermal injury-induced immunosuppression. Profound depression of cell-mediated immune response (CMIR) is a characteristic effect of burn injury, and was evaluated using the popliteal lymph node assay for graft-versus-host and host-versus-graft responsiveness in mice. Preservation of CMIR after burn injury was observed in animals treated with 40 mg/kg ibuprofen and in mice given anti-PGE antibody. It appears that PGE is a central immunoregulatory mediator of suppressed CMIR following thermal injury and that treatment resulting in inhibition of PGE production or neutralization of PGE with anti-PGE antibody prevented burn-induced immunosuppression.
Prostaglandin E (PGE) production is elevated in burn-injured individuals and has been implicated as a mechanism in thermal injury-induced immunosuppression. Profound depression of cell-mediated immune response (CMIR) is a characteristic effect of burn injury, and was evaluated using the popliteal lymph node assay for graft-versus-host and host-versus-graft responsiveness in mice. Preservation of CMIR after burn injury was observed in animals treated with 40 mg/kg ibuprofen and in mice given anti-PGE antibody. It appears that PGE is a central immunoregulatory mediator of suppressed CMIR following thermal injury and that treatment resulting in inhibition of PGE production or neutralization of PGE with anti-PGE antibody prevented burn-induced immunosuppression.